Bisphenol-A exposure induced neurotoxicity and associated with synapse and cytoskeleton in Neuro-2a cells

Yin, Zhihong; Hua, Liushuai; Chen, Lingli; Hu, Dewei; Li, Jinglong; An, Zhixing; Tian, Tian; Ning, Hongmei; Ge, Yaming

doi:10.1016/j.tiv.2020.104911

Cited by 22 publications

(22 citation statements)

References 47 publications

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“…Nonetheless, lead exposure decreased SYP protein expression in the mouse hippocampus(Yu et al 2016). In the present study, the expression of SYP was up-regulated with BPA treatment for 24 or 36 h. Similarly, the previous study showed that BPA exposure increased SYP protein expression at 150 and 200 µM for 24 h(Yin et al 2020). Further studies are required to determine the reasons why BPA induced the upregulation of SYP expression and the underlying speci c stimulated signaling pathways in Neuro-2a cells.…”

supporting

confidence: 78%

“…Cell mortality rate was measured using the LDH assay as described (Yin et al 2020). In brief, Neuro-2a cells were seeded at a density of 2 × 10 4 cells/well in 12-well plates and treated with 150 μM BPA at the designated time points, or DMSO as the solvent control.…”

Section: Cck-8 and Lactate Dehydrogenase (Ldh) Assaysmentioning

confidence: 99%

“…MAP2 is a main component of the neuronal cytoskeleton, and it promotes microtubule formation, maintains microtubule stability, regulates the formation of microtubule bundles, adjusts synaptic plasticity process, and participates in neurite formation and growth, synaptic transmission in neuronal development (Murray et al 2014). In addition, MAP2 is commonly used as a marker protein for mature neurons (Yin et al 2020). Tau is principally enriched in neuronal axons, and it physiologically promotes the assembly and stabilization of microtubules in vesicular and axonal transport (Pérez et al 2018).…”

Section: Introductionmentioning

confidence: 99%

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Bisphenol-A Exposure Induced Neurotoxicity and Synapse and Cytoskeleton Dysfunction in Neuro-2a Cells

Wang

Yin

Chen

et al. 2022

Preprint

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Bisphenol A (BPA) is one of the typical environmental endocrine disruptors. BPA was leached from polycarbonate containers into food and water, and it has been detected in collective samples from humans. Microtubule-associated protein 2 (MAP2) and Tau maintain microtubule normal function and promote the normal development of the nervous system. Synaptophysin (SYP) and drebrin (Dbn) proteins are involved in regulating synaptic plasticity. This study aimed to determine the adverse effects of BPA on Neuro-2a cells by investigating the synaptic and cytoskeletal damage. Cells were exposed to 0 (Minimum Essential Medium, MEM), 0.01% (v/v) DMSO and 150 µM BPA for 12, 24, or 36 h. Morphological analysis revealed that the cells in the BPA-treated groups shrank, collapsed, and had a reduced number of synapses compared with those in the control groups. CCK-8 and LDH assays showed that the mortality of Neuro-2a cells increased as the BPA treatment time was prolonged. Transmission electron microscopic analysis further revealed that cells demonstrated nucleolar swelling and nuclear membrane and partial mitochondrial dissolution or condensation following BPA exposure. BPA also significantly decreased the relative protein expression levels of MAP2, Tau, and Dbn (P < 0.01). Interestingly, the relative protein expression levels of SYP increased (P < 0.01). These results indicated that BPA damaged the development and proliferation of Neuro-2a cells by disrupting cytoskeleton and synaptic integrity.

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supporting

confidence: 78%

Section: Cck-8 and Lactate Dehydrogenase (Ldh) Assaysmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Bisphenol-A Exposure Induced Neurotoxicity and Synapse and Cytoskeleton Dysfunction in Neuro-2a Cells

Wang

Yin

Chen

et al. 2022

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“…NDDs, which are often behaviorally-defined, can be caused by disruptions in synaptogenesis [79]-therefore, elucidating the impacts of BPA on synapse formation is critical because of the implications for risk of neurodevelopmental impairment. Experimentally, synapse formation can be measured at the cellular and molecular level by evaluating axon growth and guidance [68,[82][83][84], dendrite length and arborization patterns [85][86][87], and expression levels of genes and proteins critical for the synaptogenic program [88]. BPA-associated deficits in synapse formation have been examined in the fruit fly [68,84], zebrafish [82,83], rodents [86][87][88], and embryonic stem cell-derived models from humans [85] (Table 4).…”

Section: Synapse Formation Is Disrupted By Bpamentioning

confidence: 99%

“…Experimentally, synapse formation can be measured at the cellular and molecular level by evaluating axon growth and guidance [68,[82][83][84], dendrite length and arborization patterns [85][86][87], and expression levels of genes and proteins critical for the synaptogenic program [88]. BPA-associated deficits in synapse formation have been examined in the fruit fly [68,84], zebrafish [82,83], rodents [86][87][88], and embryonic stem cell-derived models from humans [85] (Table 4).…”

Section: Synapse Formation Is Disrupted By Bpamentioning

confidence: 99%

Does Bisphenol A Confer Risk of Neurodevelopmental Disorders? What We’ve Learned from Developmental Neurotoxicity Studies in Animal Models

Welch¹,

Mulligan²

2022

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Substantial evidence indicates that bisphenol A (BPA), a ubiquitous environmental chemical used in the synthesis of polycarbonate plastics and epoxy resins, can impair brain development. Clinical and epidemiological studies exploring potential connections between BPA and neurodevelopmental disorders in humans have repeatedly identified correlations between early BPA exposure and developmental disorders, like attention deficit/hyperactivity disorder and autism spectrum disorder. Investigations using invertebrate and vertebrate animal models have revealed that developmental exposure to BPA can impair multiple aspects of neuronal development, including neural stem cell proliferation and differentiation, synapse formation, and synaptic plasticity—neuronal phenotypes that are thought to underpin the fundamental changes in behavior associated neurodevelopmental disorders. Consistent with BPA-associated neuronal phenotypes, behavioral analyses of BPA-treated animals have shown significant impacts on behavioral endophenotypes related to neurodevelopmental disorders, including altered locomotor activity, learning and memory deficits, and anxiety-like behavior. To contextualize the correlations between BPA and neurodevelopmental disorders in humans, this review summarizes current literature reporting on the developmental neurotoxicity of BPA in laboratory animals, with an emphasis on neuronal phenotypes, molecular mechanisms, and behavioral outcomes. The collective works described here predominantly support the notion that gestational exposure to BPA should be regarded as a risk factor for neurodevelopmental disorders.

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Integrated evaluation the antioxidant activity of epicatechin from cell dynamics

Qing

Xiang

et al. 2023

Biotechnology Progress

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Oxidative damage has been implicated in the pathogenesis of numerous disorders by affecting the normal functions of several tissues. Further, oxidative stress acts within cells to influence cell morphology and the behavior of cell migration. The movement and migration of cells are crucial during the development of organisms as they transition from embryo to adult, and for the homeostasis of adult tissues. Epicatechin (EC) is a natural flavonoid derived mostly from tea, chocolate, and red wine. We investigated the protective impact of EC on D‐galactose(D‐gal)/rotenone‐injured NIH3T3 cells and found alterations in cell dynamics throughout the procedure. The results reveal that D‐gal/rotenone stimulation can cause the cell area to expand and the number of cellular protrusions to increase. EC intervention can considerably minimize the oxidative damage of rotenone on NIH3T3 cells (p < 0.05) but showed little influence on cell damage induced by D‐gal. Furthermore, the corrective ability of EC as an antioxidant is reflected in a dose‐dependent effect on cell movement, including variations in movement speed and distance. Overall, from the perspective of cell morphology and cell motility, EC has a good protective impact on cells harmed by rotenone induced oxidative damage, as well as corrective properties as an antioxidant to balance intracellular oxidative stress, which allowing for a more comprehensive evaluation of antioxidant performance of EC.

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Bisphenol-A exposure induced neurotoxicity and associated with synapse and cytoskeleton in Neuro-2a cells

Cited by 22 publications

References 47 publications

Bisphenol-A Exposure Induced Neurotoxicity and Synapse and Cytoskeleton Dysfunction in Neuro-2a Cells

Bisphenol-A Exposure Induced Neurotoxicity and Synapse and Cytoskeleton Dysfunction in Neuro-2a Cells

Does Bisphenol A Confer Risk of Neurodevelopmental Disorders? What We’ve Learned from Developmental Neurotoxicity Studies in Animal Models

Integrated evaluation the antioxidant activity of epicatechin from cell dynamics

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